The research detailed in this application concerns itself with mechanisms involved in animal model systems of uveitis. Our hypothesis is that a small number of immunocompetant cells specific for antigen is responsible for amplification of the inflammatory response which is composed of many non-antigen-specific cells, including macrophages and lymphocytes. In our rabbit model system, we will passively immunize the eye with immunocompetent cells specific for ovalbumin or haptenic determinants using syngeneic donor lymphocytes of lymphoid tissue. Intravenous challenge with antigen or carrier protein-coupled hapten should result in uveitis. The time sequence for these experiments will allow us to demonstrate the marked immunological memory associated with uveitis, and also demonstrate T-cell help and B-cell antibody response concomitant with this recurrent ocular inflammatory disease. We feel that lymphokine products of T cells are synthesized and released after lymphocyte binding of specific antigen, and that these pharmacologically active substances are responsible nonspecific inflammatory cell accumulation. Specific anti-lymphokine antibodies will be raised in heterologous species and used in the F(ab)2 form to assess the extent and localization of lymphokines and to block nonspecific cell infiltrate. In other experiments we will attempt to augment the inflammatory component using T- and B-cell mitogens. Sea star factor (SSF) simulates many of the effector substances released from immune mechanisms of lymphokines in production of chronic ocular inflammatory lesions. Sea star factor has been demonstrated to be capable of inducing neoangiogenesis in the rabbit cornea. We will investigate the possibility that this material stimulates new vessel formation either de novo or as a result of inducing nonspecific chronic inflammation within the corneal stroma. Blockade of new vessel formation induced by SSF will be performed with extracts of cartilage and vitreous and by specific anti-SSF antibody.